Electro-acupuncture ameliorates cognitive impairment via improvement of brain-derived neurotropic factor-mediated hippocampal synaptic plasticity in cerebral ischemia-reperfusion injured rats

Abstract

A previous study by our group found that electro-acupuncture (EA) at the Shenting (DU24) and Baihui (DU20) acupoints ameliorates cognitive impairment in rats with cerebral ischemia-reperfusion (I/R) injury. However, the precise mechanism of action has remained largely unknown. The present study investigated whether brain-derived neurotropic factor (BDNF) mediates hippocampal synaptic plasticity as the underlying mechanism. Rats were randomly divided into three groups: The sham operation control (Sham) group, the focal cerebral ischemia-reperfusion (I/R) group, and the I/R with EA treatment (I/R+EA) group. The I/R+EA group received EA treatment at the Shenting (DU24) and Baihui (DU20) acupoints after the operation. EA treatment was found to ameliorate neurological deficits (P<0.05) and reduce the cerebral infarct volume (P<0.01). In addition, EA improved cognitive function in cerebral I/R-injured rats (P<0.05). Furthermore, EA treatment promoted synaptic plasticity. Simultaneously, EA increased the hippocampal expression of BDNF, its high-affinity tropomyosin receptor kinase B (TrkB) and post-synaptic density protein-95 (PSD-95) in the rats with cerebral I/R injury. Collectively, the findings suggested that BDNF-mediated hippocampal synaptic plasticity may be one mechanism via which EA treatment at the Shenting (DU24) and Baihui (DU20) acupoints improves cognitive function in cerebral I/R injured rats.

Keywords: brain-derived neurotropic factor; cerebral ischemia-reperfusion; cognitive impairment; electro-acupuncture; synaptic plasticity.

Figures

Figure 1.

Effect of EA on infarct volume. (A) T2-weighted nuclear magnetic imaging indicated cerebral infarct volume of I/R and I/R+EA groups. Red arrows indicate the infarct site. (B) Bar graph showing the infarct volume, which was quantified as a percentage of the total brain volume in each group (n=10). ##P<0.01 vs. the I/R group. I/R, ischemia-reperfusion; EA, electro-acupuncture.

Figure 2.

Effects of EA on cognitive impairment. (A) Representative tracing images from the Morris water maze test of Sham, I/R and I/R+EA groups (n=10). (B) Escape latency (duration of finding the platform within 90 sec). (C) Number of times the rats passed through the area in which the platform was located. **P#P<0.05, ##P<0.01 vs. the I/R group. I/R, ischemia-reperfusion; EA, electro-acupuncture.

Figure 3.

Effect of EA on synaptic structural plasticity. Electron microscopy images indicating the changes to synaptic ultrastructure (indicated by arrows) of the hippocampus in the (A) Sham, (B) I/R and (C) I/R+EA groups (magnification, ×50,000; n=5). I/R, ischemia-reperfusion; EA, electro-acupuncture.

Figure 4.

Effect of EA on BDNF and TrkB. (A) Western blot showing the levels of BDNF and TrkB in the hippocampus of Sham, I/R and I/R+EA groups (n=5). (B) Bar graph showing the quantified expression levels of BDNF and TrkB from each group. **P##P<0.01 vs. the I/R group. I/R, ischemia-reperfusion; EA, electro-acupuncture; BDNF, brain-derived neurotrophic factor; TrkB, tropomyosin receptor kinase B.

Figure 5.

Effect of EA on PSD-95. (A) Western blot showing the levels of PSD-95 in the hippocampus of the Sham, I/R and I/R+EA groups (n=5). (B) Bar graph showing the quantified expression levels of PSD-95 from each group. **P##P<0.01 vs. the I/R group. I/R, ischemia-reperfusion; EA, electro-acupuncture; PSD-95, post-synaptic density protein-95.